Bipolar cell

Overview

Acellinthesecondlevel(intermediate)neuronoftheretina.Thecellbodyissmallandoval,withaprotrusionextendinginwardandoutwardrespectively:theoutwardoneisdendrites,withmorebranchesattheend,formingsynapseswiththeaxonsofrodcellsandconecells;Theinwardpartisanaxon,whichformssynapseswithdifferentganglioncells.Abipolarcellisoftenassociatedwithaconecell,butitcanbeassociatedwithseveralrodcells;allexceptthemaculareceiveavisualTheexcitementofconecellsandseveralrodcellsistransmittedtolevel3neurons.

Bipolarcellsareinterneuronsinthevertebrateretina.Theyreceivesignalinputfromphotoreceptorsandtransfertoamacrinecellsandganglioncellsafterintegration.Inthetransmissionofretinalsignals,bipolarcellsdisplaytwoimportantfunctions.Oneisthroughthedifferentglutamatereceptorsonitsdendritestoshuntthevisualsignalintolight(ON)andwithdraw(OFF)signals;theotheristhroughitsspecialsynapseswithamacrinecellsandganglioncells.Thecontacttransmissionmethodconvertsthecontinuousgradedpotentialintotransientneuralactivity.

Synaptictransmissionmechanism

Bandsynapses

Theaxonterminalsofbipolarcellsandpostsynapticneuronsmainlyformbandsynapses(ribbonsynapse),whichischaracterizedbyadensebandorrodattheterminal,atrightanglestothepresynapticmembrane,withadepthofabout1μm,usuallylocatedinorontheouterprotrusionridgeoftheterminalmembrane,betweenthebandandtheridgemembraneThetapeistiedtothemembranebyabow-shapeddensecordinbetween.Synapticvesiclesaredelicatelyarrangedaroundthesynapticband,andtherearefilamentsconnectedbetweenthebandandthevesicles.Onbothsidesoftheprotrudingridge,thevesiclescanfusewiththemembrane,andtheband-shapedstructuremayactasachannelinthisprocess.Thisstructureisobviouslydifferentfromtheusualsynapse(conventionalsynapse).Bandsynapsesarealsofoundinothersensoryneurons,suchasphotoreceptorsandcochlearhaircells.Afterthesynapse,thereareusuallytwopostsynapticprotrusions(dimers),eitherbothofwhichareamacrinecellprotrusions,oroneisaganglioncelldendritesandtheotherisamacrinecellprotrusions.Thispost-synapticconcatenationstructureisalsoseeninothersensoryneuronbandsynapses.

Exocytosisofbandsynapses

Bipolarcellsuseglutamateasatransmitter.Whenthetransmitterisreleased,synapticvesiclesandpresynapticmembranefuse(cellSpit),causingthesurfaceareaof​​theanteriormembranetoincrease;andwhenthefusedvesiclemembranereturnstothecell(endocytosis),itwillcausethesurfaceareaof​​theanteriormembranetodecrease.

Endocytosisofbandsynapses

Theeffectivetransmissionofsynapticsiteinformationmusthavethevesiclemembraneintegratedintothepresynapticmembranetoeffectivelyrecycle(endocytosis),otherwiseTheareaof​​thepresynapticmembranewillcontinuetoincrease,andthereleasablevesiclesinthesynapticactiveareawillgraduallydecrease.Calciumalsoplaysanimportantregulatoryroleinthere-recoveryofvesiclemembranesafterneurotransmitterrelease.Increasingtheintracellularcalciumconcentrationcanstronglyinhibittheoccurrenceofterminalendocytosisinbipolarcells.Whentheintracellularcalciumconcentrationis0.8-20μmol/L,itsexocytosisandendocytosisaremaintainedinafastandbalancedcycle(about900vesicles/s).Itcanbeseenthattheroleofcalciuminthesignaltransmissionofbandsynapsesiscrucial.Itcoordinatestheprocessesoftransmitterrelease,vesiclere-recovery,andvesiclelibraryreplenishment.Studyingtheregulationmechanismofintracellularcalciumconcentrationonsynapticvesiclecirculationwillundoubtedlycontributetothein-depthunderstandingofsynapticevents.StudieshaveshownthatNa-Caexchange,theactivityofplasmamembranecalciumpumps,andtheuptakeofintracellularfreecalciumbymitochondriaplayanimportantroleintheregulationofintracellularcalciumconcentrationinbipolarcells.

Clinicaldiseases

Retinaldegenerativediseasesareseriousdiseasesthatcauseblindnessinhumanstoday.

(1)Themorphologicalchangesofbipolarcellsduringretinaldegeneration

10～afterbirthIn20drd10miceandwild-typemice,thereisnodifferenceinthemorphologyandlevelofbipolarcells.Thecellbodyiselliptical,thedendritesaredendriticanddense,andtheaxonsareverylong,extendingintotheinnerreticularlayer(innerplexiformlayer(IPL)deeplayer.Inrd10mice25daysafterbirth,themorphologyofbipolarcellsbegantochange.Thetreeofretinalbipolarcells(RBCs)hasashortermutation,andthisdifferenceismorepronouncedinthecenteroftheretinathanintheperipheralarea.Thirtydaysafterthebirthofrd10mice,asthephotoreceptorcellsdegenerated,thedendriticretractionofRBCsbecamemoreobvious.Inrd10mice45daysafterbirth,thedendritesofRBCsremainedonlyalittleintheperipheralareaof​​theretina,whiledendritesdisappearedinthecentralarea.Somescholarshavediscoveredthatduringtheremodelingprocessofretinaldegenerativebipolarcells,RBCsandconeshaveashort-termdislocationconnection.

(2)Functionalchangesofbipolarcellsintheprocessofretinaldegeneration

Duringtheprocessofphotoreceptorcelldegeneration,ThelightresponseofONbipolarcellsgraduallydisappeared,thecationchannelregulatedbyglutamatereceptorswasclosed,themGluRresponsedisappearedorremainedunchanged,andtheiGluRresponseappearedorincreased;theiGluRresponseofOFFbipolarcellsremainedunchangedordisappeared.